Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study included 200 patients with pleural effusion. Pleural effusions were transudative in 48 (24%) and exudative in 152 (76%) of cases. Congestive cardiac failure (14.5%), nephrotic syndrome (5.5%), and liver cirrhosis (2.5%) were the most common etiological diagnoses of transudate cases. Malignant effusion (16.5%), pneumonia (13%), pleural empyema (9%), tuberculosis (6%), and pulmonary embolism (5.5%) were the most common etiological diagnoses of exudative cases. Thirty-two (16%) cases of exudative pleural effusions were of undertermined etiology. Polymorphonuclear leucocytes predominated in 48 patients with exudative pleural effusions. The most common etiological diagnoses were pneumonia (41.67%), pleural empyema (39.59%) and pulmonary embolism (10.42%). Lymphocytes in pleural fluid were predominant in 63 patients, with malignant (6.34%), tuberculous pleurisy (19.02%), pulmonary embolism (6.34%), trauma (6.34%), and (46.11%) cases in patients with pleural exudate undertermined etiology. Eosinophyls were predominant in 16 (8%) patients with exudative pleural effusions. The most common etiology of eosinophilic pleural fluid were pneumonia (37.5%), malignant pleural effusion (25%), pulmonary embolism (12.5%), pyopneumothorax (6.25%) and trauma 6.25%. From 16 patients with eosinophilic pleural exudate, in 31% cases air, in 12.5% blood in pleural fluid were determined and in 12.5% cases previous pleural puncture was performed. Pleural fluid eosinophilia is most commonly associated with the presence of air or blood in the pleural fluid (correalation index 0.82). Malignant pleural effusions were determined in 33 patients. Malignant cells in pleural fluid were identified in 25 cases. The diagnostic sensitivity of pleural fluid cytology for malignant pleural effusions were 76%. Hemoragic pleuritis was determined in 18 and hemothorax in 4 patients. Etiology of hemothorax were trauma (75%) and coaguliopathia (25%). Most common etiological diagnoses of hemoragic pleuritis were neoplasia (33.3%), pulmonary embolism (16.65%), trauma (16.65%), pneumonia (11.11%), and congestive cardiac failure (11.11%). Diagnostic sensitivity and specifity of hemoragic pleuritis is low, 58% and 45% respectively.
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PMID:[Diagnostic value of pleural fluid cytologic examination]. 1255 57

Incidence data on thromboembolism in patients with heart failure (which may include stroke, peripheral embolism, pulmonary embolism) are limited but provide a general population range from 1-5 cases per 1000 each year, increasing with age to more than 30 cases per 1000 each year among people aged 75 years or older. However, the incidence of thromboembolism varied depending very much on what was being investigated in each of these studies. Data from subgroup analysis of the larger heart failure trials would seem to support this incidence data, although there is very little true epidemiological data and no randomised, controlled trial has been designed to specifically investigate thromboembolism in patients with heart failure. The pathophysiology of heart failure is complex. There are many well recognised factors which are associated with thrombosis in heart failure patients, such as vascular abnormalities, increased coagulability and impaired blood flow. In the past 50 years many studies have been performed to investigate if oral anticoagulation is of benefit for the prevention of thromboembolism in patients with heart failure. The use of warfarin therapy for heart failure patients has been a controversial subject. Warfarin does have a role to play in patients with myocardial infarction and those with atrial fibrillation. Furthermore, in patients with congestive heart failure secondary to coronary artery disease, warfarin reduces the occurrence of nonfatal myocardial infarction and, therefore, may reduce the chances of progression to heart failure. It has also been shown that warfarin reduces the risk of thromboembolic strokes in patients recovering from myocardial infarction. At present, there is a lack of randomised data, and the incidence of bleeding complications in patients with heart failure has caused a decrease in the use of oral anticoagulants for the prevention of thrombosis. This review summarises the incidence, potential mechanism and therapeutic approaches for management of thromboembolism in heart failure.
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PMID:Blood coagulation in patients with chronic heart failure: evidence for hypercoagulable state and potential for pharmacological intervention. 1265 54

The use of B-type natriuretic peptide to diagnose congestive heart failure is becoming more frequent and widespread. We report five patients recently seen at our hospital who were diagnosed with pulmonary embolism and noted to have elevated B-type natriuretic peptide levels. We caution that elevations of B-type natriuretic peptide may in some patients have the potential to mislead clinicians if the diagnosis of pulmonary embolism is not considered.
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PMID:Elevations of B-type natriuretic peptide in pulmonary embolism: a case series. 1465 83

B-type natriuretic peptide is a neurohormone secreted from the cardiac ventricles in response to ventricular stretch and pressure overload. It counteracts the vasoconstriction that occurs as a compensatory mechanism in heart failure. A new test for measuring plasma levels of B-type natriuretic peptide can help in the diagnosis and treatment of patients with congestive heart failure. Dyspnea associated with cardiac dysfunction is highly unlikely in patients with levels of the peptide less than 100 pg/mL. Whereas most patients with significant congestive heart failure have levels of the peptide greater than 400 pg/mL, in patients with levels of 100 to 400 pg/mL, left ventricular dysfunction without volume overload, pulmonary embolism, and cor pulmonale must be ruled out. Thus, incorporating measurement of B-type natriuretic peptide into clinical evaluation helps physicians and nurses diagnose heart failure more quickly, especially in patients who have multiple comorbid conditions. Elevated levels of B-type natriuretic peptide indicate a poor prognosis in terms of a higher mortality and more hospital readmissions. Levels of B-type natriuretic peptide could be used to guide therapy and discharge planning for patients admitted with decompensated heart failure.
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PMID:B-type natriuretic peptide: a diagnostic, prognostic, and therapeutic tool in heart failure. 1473 47

The Japanese Society of Anesthesiologists (JSA) conducts an annual survey of life-threatening events in operating rooms (OR) in JSA Certified Training Hospitals (JSACTH) by sending and collecting confidential questionnaires. Etiologies of the incidents were divided into four categories: those totally attributable to anesthetic management (AM), those resulting from preoperative complications (PC), those resulting from intraoperative pathological events (IP) and those related to surgical procedures (SP). IP resulted from coronary ischemia not suspected preoperatively, arrhythmias, pulmonary embolism, and other conditions. Outcomes were judged on the 7th post-operative day. In the year 2002, questionnaires were sent to 844 JSACTHs, and a total of 1,461,020 cases of anesthesia were documented from 773 JSACTHs. Of these, 1,277,045 cases of anesthesia from 712 JSACTHs were available for analysis. Seven hundred thirty nine cardiac arrests (5.79 per 10,000 anesthetics) and 806 deaths (6.31 per 10,000 anesthetics) due to life-threatening events in the OR were reported. The incidence of cardiac arrest and mortality totally attributable to AM was 0.38 and 0.11 per 10,000 anesthetics. These values tended to decrease after 1994, except the mortality totally attributable to AM, which were almost at constant level during recent years. The summary of the study between 1999 and 2002 was as follows. Among 3,855,384 anesthetics, 2,443 cardiac arrests (6.34 per 10,000 anesthetics) and 2,638 deaths (6.85 per 10,000 anesthetics) due to life-threatening events in the OR were reported. PC, SP, IP and AM were responsible for 64.7, 23.9, 9.4, and 1.5% of deaths, respectively. The major cause of PC related deaths was preoperative hemorrhagic shock, followed by cardiovascular diseases such as myocardial ischemia and congestive heart failure. Excessive surgical bleeding comprised 70.2% of SP-related deaths. The major causes of IP-related death were myocardial ischemia, pulmonary embolism, and severe arrhythmias. The incidence of cardiac arrest and death totally attributable to AM was 0.47 and 0.10/10,000 anesthetics, respectively. Among patients with ASA-PS 1(E) and 2(E), AM-related deaths occurred at a rate of 0.04/10,000 anesthetics. Half of AM-induced deaths were caused by airway or ventilatory problems. Other causes of AM-related death were medication accidents and infusion/transfusion accidents. Considerable effort is required to reduce intraoperative life-threatening events caused by human error, hemorrhage, and cardiovascular diseases.
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PMID:[Annual mortality and morbidity in operating rooms during 2002 and summary of morbidity and mortality between 1999 and 2002 in Japan: a brief review]. 1507 89

We hypothesize that the pathophysiology of many cardiovascular diseases reflects a maladaptation of the triad of trauma response: adrenergia, inflammation, and coagulation. During biologic evolution, trauma has likely been a prevailing factor in natural selection. Components of the trauma triad act to limit hemorrhage, defend wounds against microorganisms, and initiate reconstruction. Response pathways that enable survival after trauma confer obvious adaptive advantages especially if the individual goes on to reproduce. Modern humans have shaped their own ecologic environment in such a way that the incidence of trauma has waned and previously unseen pathologies have emerged. Manifestations of modern diet, changing lifestyles, and extended lifespan have suddenly created new pathologic challenges to our prehistoric physiologic system. During our evolutionary heritage, endothelial injury and end-organ hypoxia were likely exclusively associated with physical trauma and the responses of the trauma triad were appropriate. Today, endothelial injury is more often precipitated by distinctly modern stressors such as hypertension, smoking, diabetes, and dyslipidemia. The once-adaptive trauma response can maladaptively initiate dangerous, self-propelling cycles of adrenergia, inflammation, and coagulation. Acute coronary syndromes perhaps best exemplify this phenomenon. Congestive heart failure, which often ensues, can similarly be seen as a maladaptation of the trauma triad. Whereas end-organ hypoxia was once commonly associated with trauma, now hypoxia is more often attributable to distinctly modern stressors such as pump failure. The fluid conservation and inflammation that results from the trauma triad was clearly adaptive in our prehistoric past, but in congestive heart failure the response is maladaptive, engendering self-propelling exacerbations of pump failure and vascular disease. Our maladaptive trauma response hypothesis portends new diagnostic and therapeutic paradigms for cardiovascular diseases and has ramifications for many other conditions such as stroke, venous thrombosis, vasculitis, aortic disease, arterial disease, pulmonary embolism, and restenosis.
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PMID:Acute coronary syndromes and heart failure may reflect maladaptations of trauma physiology that was shaped during pre-modern evolution. 1514 37

Anthracyclines, found to be efficacious in the treatment of a broad spectrum of pediatric malignancies, are cardiotoxic and may lead to heart failure even a long time after successful treatment of cancer. It is thought that subtle abnormalities can progress to the more permanent myocardial disease, resulting in cardiomyopathy which may progress to congestive heart failure. There are some precipitating factors leading to the sudden onset of cardiac symptoms such as increase in afterload or preload. We describe a young patient with congestive heart failure treated with doxorubicin (cumulative mean dose 420 mg/m2) in infancy because of pelvic sarcoma in whom the appearance of symptoms was related to pulmonary embolism. Four years before hospital admission, the patient presented echocardiographic abnormalities such as left ventricular fractional shortening and thickness reduction and he was treated with ACE-inhibitors. The myocardial ischemia, which is present in pulmonary embolism, probably worsened the left ventricular systolic function and caused congestive heart failure.
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PMID:[Biventricular heart failure in patient treated with anthracycline in childhood: myocardial dysfunction is not always the cause]. 1518 68

Acute occlusion of an abdominal aortic aneurysm is a rare phenomenon. Its possible complications include distal spasm followed by arterial thrombosis, ischemia of the distal limbs, distal embolization, acidosis, hyperkalemia, and the development of venous thrombosis of the lower limbs. Surgical correction is often complicated by cardiac decompensation, renal failure, fatal pulmonary embolism, and metabolic derangements related to toxins released from the revascularized limb. Unless contraindicated, immediate systemic heparinization must be undertaken when the diagnosis is first suspected. We present a case of sudden occlusion of an abdominal aortic aneurysm complicated by venous thrombosis involving both lower extremities. After undergoing surgical revascularization, the patient sustained massive fatal pulmonary emboli. Prophylactic interruption of the inferior vena cava may be indicated in patients who present with this complication of abdominal aortic aneurysm.
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PMID:Acute occlusion of an abdominal aortic aneurysm complicated by bilateral lower extremity venous thrombosis: A case report. 1521 31

The purpose of the study was to evaluate the prevalence of atelectasis as an alternative diagnosis in patients who underwent computed tomographic pulmonary angiography (CT-PA) for suspected pulmonary embolism (PE), and to contrast the pathophysiology of pulmonary atelectasis and PE, both of which are associated with dyspnea and hypoxemia. We retrospectively identified 144 consecutive emergency department patients (n=49) and inpatients (n=95) admitted between July 2001 and June 2002 who were evaluated with CT-PA for suspected PE. There were 98 women and 46 men with a mean age of 58 years (range 27-95 years). Each CT report was reviewed for PE, the words "atelectasis," "collapse," and/or "volume loss," findings known to predispose to atelectasis, and alternative diagnoses. CT scans of those with PE and those with atelectasis were reviewed. Each case was categorized into one of three groups, as follows: group 1, PE; group 2, atelectasis of three or more segments and no PE; group 3, neither PE nor atelectasis. PaO2 was documented, when available (n=115), with PaO2 >100 mmHg recorded as 100 mmHg. Reports for group 3 were reviewed for alternative diagnoses. Thirteen percent of the study population (19/144, group 1) had PE, and two of them had concomitant atelectasis; mean PaO2 was 69 mmHg (range 38-100 mmHg). Nineteen percent of the study population (27/144, group 2) had atelectasis of three or more segments without PE; mean PaO2 was 73 mmHg (range 45-100 mmHg). Sixty-eight percent of the study population (98/144, group 3) had neither PE nor atelectasis; mean PaO2 was 79 mmHg (range 36-100 mmHg). There was a significant difference in the PaO2 between groups 1 and 3 (Student's t-test), with group 2 intermediate. Seventy percent of group 2 (19/27) had at least one finding predisposing to atelectasis: central bronchial abnormality (n=6), moderate or larger pleural effusion (n=11), pleural mass, pneumothorax, elevated hemidiaphragm, and severe kyphosis (the last four all n=1 each), versus 16% (3/19) of group 1 ( P<0.05). Sixty-three percent of group 3 (62/98) had one or more alternative diagnoses on CT that explained the patient's symptoms as follows: pneumonia (28%, 27/98), other lung disease (18%, 18/98), congestive heart failure (13%, 13/98), and malignancy (13%, 13/98). Pulmonary atelectasis was common in patients undergoing CT-PA for suspected PE, equaling pneumonia as the most common alternative diagnosis. Most patients with atelectasis had predisposing findings on CT. Pulmonary atelectasis and PE cause similar symptoms by different mechanisms of ventilation-perfusion mismatch.
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PMID:Pulmonary atelectasis: a frequent alternative diagnosis in patients undergoing CT-PA for suspected pulmonary embolism. 1529 Apr 80

A phase II trial at 12 institutions using AT (doxorubicin 60 mg/m2 plus docetaxel 60 mg/m2) given every 21 days was conducted. Eighty-nine patients were entered who ranged in age from 25 to 75 years, 41.6% of whom had stage IIIB disease and 58.4% of whom had stage IV disease. Among the patients with stage IV disease, 32.7% had received prior adjuvant chemotherapy. Premedication with dexamethasone (8 mg orally twice per day for 3 days) and prophylactic ciprofloxacin (500 mg orally twice per day on days 5-15) was used. Colony-stimulating growth factors were reserved for secondary prophylaxis after prolonged or febrile neutropenia (FN) or documented severe infection in an earlier cycle. After a cumulative dose of doxorubicin of 480 mg/m2, patients could continue to receive docetaxel (100 mg/m2) alone. Median time on study as of July 6, 2003, was 54 months. Febrile neutropenia occurred in 36 patients (41.9%): 23 developed FN in the absence of previous prophylactic growth factor support and 13 developed it despite previous growth factor support. One patient died from sepsis. Other grade 3/4 adverse events included nausea in 3.5%, vomiting in 4.7%, stomatitis in 8.1%, diarrhea in 5.8%, arthralgia/myalgia in 2.3%, fluid retention in 1.2%, pulmonary embolism in 1.2%, rest dyspnea in 1.2%, neuromotory toxicity in 1.2%, and neurosensory toxicity in 1.2%. Clinical congestive heart failure was seen in 2 patients (2.3%). Sixty-seven patients were evaluable for best response with 6 cycles of therapy. Fourteen patients (20.9%) had a complete response and 30 (44.8%) had a partial response, for an overall response rate of 65.7% in evaluable patients. The median response duration was 25.9 months, and the median time from entry to progression or death was 27.5 months. The median survival time for the 86 patients with endpoint information was 31.1 months. The administration of AT with primary ciprofloxacin and secondary colony-stimulating factor prophylaxis is feasible, and the combination is active. Its value in the adjuvant setting is currently under investigation.
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PMID:Phase II trial of a doxorubicin/docetaxel doublet for locally advanced and metastatic breast cancer: results from national surgical adjuvant breast and bowel project trial BP-57. 1533 53


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